New Study: Discovery of new pathway in brain has implications for schizophrenia treatment

The NMDAR is the most investigated receptor in neuroscience because it is essential to synaptic plasticity, which is instrumental in establishing and remodeling brain circuitry and is thought to be the cellular foundation of learning and memory," said Thomas Papouin, Ph.D., research assistant professor at Tufts School of Medicine and lead author of the study. "The NMDAR is known to be activated by two chemicals: glutamate, which is supplied by neurons, and D-serine, which is supplied by astrocytes. While most research is focused on the role that neurons play in activating the NMDAR via glutamate, we focused on the role played by astrocytes through the release of D-serine.

“This is an exciting finding with direct relevance to development of new treatments for schizophrenia, which is characterized by low levels of D-serine and diminished NMDAR as well as a major loss of cholinergic function. Efforts to develop pharmaceuticals to address these deficits have so far been unsuccessful, but in our study we were able to enhance NMDAR function via D-serine by stimulating a7nAChRs with a drug that has been part of recent stage 3 clinical trials for schizophrenia,” said Philip G. Haydon, Ph.D., corresponding author on the paper, the Annetta and Gustav Grisard professor and chair of the Department of Neuroscience at Tufts School of Medicine, and a member of the neuroscience program faculty at the Sackler School of Graduate Biomedical Sciences at Tufts. “This suggests that cholinergic drugs now under development for schizophrenia work through this newly discovered astrocytic pathway.”

Read more at: https://medicalxpress.com/news/2017-05-discovery-pathway-brain-implications-schizophrenia.html#jCp

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This findings is particularly for enhancing cognitive impairment…

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Is this related to sarcosine and why it might work?

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@insidemind I think it’s related to Encenicline. Never read somewhere that Sarcosine or Bitopertin has effects on a7nAChRs receptors.

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Wouldn’t it be amazing if big pharma actually produced a medicine that they knew how it worked.

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so nicotinic agonists enhance nmda
very interesting

is there some strong agonists thats readily available today?

i tried once wellbutrin 300mg which at that dose should have decent antagonistic effect at said nicotinic receptor
results? i couldnt think at all… i had thought blockade
it was like my ability to synthesize diminished

Galantamine  

ive read about it before but couldnt get a prescription
and wiki isnt clear on nefiracetam but i could try that one i guess

i wonder how those agonists behave when patient is heavy smoker like i am

I’ve tried Nefiracetam and it masked symptoms. What I mean, it makes you feel drugged and symptom free for a couple of hours than the symptoms return quite hard.

all meds works like that
antipsychotics are great example

if you want a real cure you would need a serious rewiring of your brain on a molecular level
lets toss in some (epi)genetic makeover too

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I tried galantamine for two or three weeks and felt some small improvement in my coherence. Usually I am completely dysfluent due to alogia. In studies galantamine has not had any proven efficacy for negative symptoms in general, however it has been shown to have some effect on alogia symptoms.

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